Abstract
Disseminated intravascular coagulation (DIC) is a syndrome characterized by systemic
intravascular activation of coagulation, leading to a widespread deposition of fibrin
in the circulation. There is ample experimental and pathological evidence that the
fibrin deposition contributes to multiple organ failure. The massive and ongoing activation
of coagulation may result in depletion of platelets and coagulation factors, which
may cause bleeding (consumption coagulopathy). The syndrome of DIC is well known in
the medical literature for centuries, although a more precise description of the underlying
mechanisms had to await the 20th century. Initial ideas on a role of the contact activation
system as the primary trigger for the systemic activation of coagulation as well as
a presumed hyperfibrinolytic response in DIC have been found to be misconceptions.
Experimental and clinical evidence now indicate that the initiation of coagulation
in DIC is caused by tissue factor expression, which in combination with downregulated
physiological anticoagulant pathways and impaired fibrinolysis leads to widespread
fibrin deposition. In addition, an extensive bidirectional interaction between coagulation
and inflammation may further contribute to the pathogenesis of DIC.
Keywords
disseminated intravascular coagulation - history - microvascular thrombosis - tissue
factor - coagulation inhibitors - fibrinolysis - inflammation
